Search results for: Glucose Transporter 1
#35751762 2022/06/25 To Up
A Narrative Review of Diabetic Kidney Disease: Previous and Current Evidence-Based Therapeutic Approaches.Diabetic kidney disease (DKD) is one of the most important diabetic complications. DKD is also the most common cause of chronic kidney disease (CKD) and end-stage renal disease. This review focused on potential therapeutic drugs for which there is established evidence of treatment for DKD. The earliest evidence for DKD treatment was established with renin-angiotensin system (RAS) inhibitors; however, their efficacy was partial. Recently, the sodium-glucose co-transporterÂ 2 (SGLT2) inhibitors, including empagliflozin (EMPA-REG Outcome), canagliflozin (CREDENCE trial), and dapagliflozin (DAPA-CKD), demonstrated a significant and clinically relevant reduction in the risks of albuminuria and progression of nephropathy, doubling of serum creatinine levels, and initiation of renal replacement therapy. Additionally, incretin-based therapeutic agents, such as glucagon-like peptideÂ 1, liraglutide (LEADER), and dipeptidyl peptidaseÂ 4 inhibitors, linagliptin (CARMERINA) have elicited vasotropic actions, suggesting a potential for reducing the risk of DKD. Until recently, mineralocorticoid receptor antagonists (MRAs) have not been suitable for DKD treatment because of their adverse effect of hyperkalemia. In contrast, finerenone, a non-steroidal MRA, significantly reduced renal composite endpoint without severe hyperkalemia that would force its discontinuation (FIDELIO-DKD). Thus, the mainstay treatments of DKD are RAS inhibitors, SGLT2 inhibitors, incretin-based therapeutic agents, and non-steroidal MRA, or in other words, the DKD "fantastic four".
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#35750011 2022/06/21 To Up
Hypouricemic effect of 2,4-dihydroxybenzoic acid methyl ester in hyperuricemic mice through inhibiting XOD and down-regulating URAT1.In this paper, we reported the hypouricemic effect of 2,4-dihydroxybenzoic acid methyl ester (DAE), a component of Ganoderma applanatum, in hyperuricemic mice through inhibiting XOD and down-regulating URAT1. Computationally, DAE showed a high similarity to allopurinol and depicted a high affinity in docking to XOD. In vitro, DAE exhibited an inhibitory effect against XOD. Importantly, DAE demonstrated a remarkable hypouricemic effect, decreasing serum uric acids (SUAs) of hyperuricemic mice (407Â Â±Â 31 Î¼mol/L) to 195Â Â±Â 23, 145Â Â±Â 33 and 134Â Â±Â 16 Î¼mol/L (PÂ <Â 0.01) at the doses of 20, 40, and 80Â mg/kg with a dose-dependent manner and showing efficacies at 54-68Â %, which were close to the efficacies of allopurinol (61Â %) and benzbromarone (57Â %). DAE depicted higher and negatively dose-independent urinary uric acids in comparison with that of the hyperuricemic control, implying DAE exerted an uricosuric effect and also a reduction effect on uric acid production. Unlike toxic allopurinol and benzbromarone, no general toxicity on body weights and no negative influence on liver, kidney, spleen and thymus were observed for DAE. Mechanistically, DAE inhibited XOD activities in vivo. Moreover, DAE up-regulated OAT1 and down-regulated GLUT9, URAT1 and CNT2. Overall, DAE may present a hypouricemic effect through inhibiting XOD and up-regulating OAT1 and down-regulating GLUT9, URAT1 and CNT2. This work provided novel insights into the hypouricemic effect of DAE and G. applanatum.
Tianqiao Yong, Danling Liang, Chun Xiao, Longhua Huang, Shaodan Chen, Yizhen Xie, Xiong Gao, Qingping Wu, Huiping Hu, Xiangmin Li, Yuancao Liu, Manjun Cai
1559 related Products with: Hypouricemic effect of 2,4-dihydroxybenzoic acid methyl ester in hyperuricemic mice through inhibiting XOD and down-regulating URAT1.10 mg10 mg25 mg25 mg25 mg50 mg1 g10 mg100 mg1 mg100 mg25 mg
#35747316 2022/01/12 To Up
Foundational drugs for HFrEF: the growing evidence for a rapid sequencing strategy.In randomised, placebo- or active-controlled trials in patients with heart failure with reduced ejection fraction (HFrEF), each of the combination of a neprilysin inhibitor and an angiotensin-receptor blocker (i.e. sacubitril/valsartan), a beta blocker, a mineralocorticoidreceptor antagonist and a sodium-glucose co-transporter 2 (SGLT2) inhibitor have been shown to reduce morbidity and mortality, firmly establishing the role of these five agents, prescribed as four pills, as foundational therapy for HFrEF. Traditionally, the guideline-advocated strategy for the initiation of these therapies was based on the historical order in which the landmark clinical trials were performed, and the requirement to uptitrate each individual drug to the target dose (or maximally tolerated dose below this) prior to initiation of another therapy. This process could take six months or more to complete, during which time patients would not be taking one or more of these life-saving drugs. Recently an alternative, evidence-based, rapid three-step sequencing strategy has been proposed with the aim of establishing HFrEF patients on low-doses of all four foundational treatments within four weeks. This strategy is based on the premise that the benefits of each of these therapies are independent and additive to the others, the benefits are apparent at low doses early following initiation, and a specific ordering of therapies may increase likelihood of tolerance of others. This article will outline this novel rapid-sequencing strategy and provide an evidence-based framework to support its adoption into clinical practice.
Kieran F Docherty, John J V McMurray
2445 related Products with: Foundational drugs for HFrEF: the growing evidence for a rapid sequencing strategy.100 tests 1 G5 g1 ml 100ul100 mg1 mg100 mg0.2 mg1.0 mg 1 G
#35744783 2022/06/07 To Up
The Ameliorative Effect of Empagliflozin in Vigabatrin-Induced Cerebellar/Neurobehavioral Deficits: Targeting mTOR/AMPK/SIRT-1 Signaling Pathways.Vigabatrin (VGB) is an antiepileptic drug that acts to irreversibly inhibit the Î³-aminobutyric acid (GABA) transaminase enzyme, elevating GABA levels. Broad studies have established that long-term treatment and/or high doses of VGB lead to variable visual defects. However, little attention has been paid to its other side effects, especially those demonstrating cerebellar involvement. Sodium glucose-linked co-transporter 2 (SGLT2) inhibitors are antidiabetic agents with protective effects far greater than expected based on their anti-hyperglycemic effect. Our study herein was designed to investigate the possible ameliorative effect of empagliflozin, the SGLT2 inhibitors, in VGB-induced cerebellar toxicity. A total of 40 male Wistar rats were allocated equally into 4 groups: : control group; : VGB group; empagliflozin treated VGB group; and : empagliflozin treated group. All groups were subjected to the detection of cerebellar messenger RNA gene expression of silent mating type information regulation 2 homolog 1 (SIRT1) and Nucleoporin p62 (P62). Mammalian target of rapamycin (mTOR), adenosine monophosphate-activated protein kinase (AMPK), and beclin1 levels were assessed by the ELISA technique while malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were detected spectrophotometrically. Immuno-histochemical studies, focusing on glial fibrillary acidic protein (GFAP) and S100 were performed, and the optical color density and the mean area percentage of GFAP positive astrocytes and the number of S 100 positive cells were also counted. Following empagliflozin treatment, we documented significant upregulation of both SIRT1 and P62 mRNA gene expression. Additionally, AMPK, Beclin1 levels, and SOD activity were significantly improved, while both mTOR and MDA levels were significantly reduced. We concluded for the first time that empagliflozin efficiently ameliorated the VGB-induced disrupted mTOR/AMPK/SIRT-1 signaling axis with subsequent improvement of the autophagy machinery and mitigation of the oxidative and inflammatory cellular environment, paving the way for an innovative therapeutic potential in managing VGB-induced neurotoxicity.
Rabab M Amer, Amira Kamel Eltokhy, Rasha Osama Elesawy, Amany Nagy Barakat, Eman Basha, Omnia Safwat Eldeeb, Alshimaa Aboalsoud, Nancy Mohamed Elgharabawy, Radwa Ismail
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#35742943 2022/06/10 To Up
Hypertension and Type 2 Diabetes-The Novel Treatment Possibilities.Elevated blood pressure and hyperglycaemia frequently coexist and are both components of metabolic syndrome. Enhanced cardiovascular risk is strongly associated with diabetes and the occurrence of hypertension. Both hypertension and type 2 diabetes, if treated inappropriately, lead to serious complications, increasing the mortality of patients and generating much higher costs of health systems. This is why it is of great importance to find the missing link between hypertension and diabetes development and to simultaneously search for drugs influencing these two disorders or even drugs aimed at their pathological bases. Standard antihypertensive therapy mainly focuses on blood pressure reduction, while novel drugs also possess a wide range of pleiotropic modes of actions, such as cardio- and nephroprotective properties or body weight reduction. These properties are especially desirable in a situation when type 2 diabetes coexists with hypertension. This review describes the connections between diabetes and hypertension development and briefly summarises the current knowledge regarding attempts to define targets for the treatment of high blood pressure in diabetic patients. It also describes the standard hypotensive drugs preferred in patients with type 2 diabetes, as well as novel drugs, such as finerenone, esaxerenone, sodium-glucose co-transporter-2 inhibitors, glucagon-like peptide-1 analogues and sacubitril/valsartan.
Agnieszka Przezak, Weronika Bielka, Andrzej Pawlik1200ul1200ul5/100 Packing /sleeve/bo200ug200ul200ul200ug200ul96T
#35741869 2022/06/07 To Up
Valorizing Coffee Silverskin Based on Its Phytochemicals and Antidiabetic Potential: From Lab to a Pilot Scale.This study investigates the possibility of valorizing coffee silverskin through the recovery of its bioactive compounds using a sustainable extraction method that could be industrially applied. For that, aqueous extracts were prepared using ultrasonic-assisted extraction (laboratorial scale) and, for comparison, a scale-up of the process was developed using the Multi-frequency Multimode Modulated technology. A concentration procedure at the pilot scale was also tested. The three types of extracts obtained were characterized regarding caffeine and chlorogenic acids contents, and the effects on intestinal glucose and fructose uptake (including sugar transporters expression) in human intestinal epithelial (Caco-2) cells were ascertained. The phytochemical contents of the extracts prepared at the laboratory and pilot scale were comparable (caffeine: 27.7 vs. 29.6 mg/g freeze-dried extract; 3-, 4-, and 5-caffeoylquinic acids: 0.19 vs. 0.31, 0.15 vs. 0.42, and 1.04 vs. 1.98 mg/g, respectively; 4- and 5- feruloylquinic acids: 0.39 vs. 0.43 and 1.05 vs. 1.32 mg/g, respectively). Slight differences were noticed according to the extracts preparation steps, but in general, all the extracts promoted significant inhibitions of [1,2-H(N)]-deoxy-D-glucose and C-D-fructose uptake, which resulted mainly from a decrease on the facilitative glucose transporter 2 (GLUT2) and sodium-glucose linked transporter 1 (SGLT1) genes expression but not on the expression of the facilitative glucose transporter 5 (GLUT5) gene. Moreover, a synergistic effect of caffeine and 5-caffeoylquinic acid on sugars uptake was found. The results clearly show that the Multi-frequency Multimode Modulated technology is a viable option to be applied at an industrial level to recover bioactive components from silverskin and obtain extracts with antidiabetic potential that could be used to develop functional food products or dietary supplements.
Juliana A Barreto Peixoto, Nelson Andrade, Susana Machado, Anabela S G Costa, Helder Puga, Maria Beatriz P P Oliveira, FÃ¡tima Martel, Rita C Alves
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#35740974 2022/06/19 To Up
Neuroprotective Effects of Pharmacological Hypothermia on Hyperglycolysis and Gluconeogenesis in Rats after Ischemic Stroke.Stroke is a leading threat to human life. Metabolic dysfunction of glucose may play a key role in stroke pathophysiology. Pharmacological hypothermia (PH) is a potential neuroprotective strategy for stroke, in which the temperature is decreased safely. The present study determined whether neuroprotective PH with chlorpromazine and promethazine (C + P), plus dihydrocapsaicin (DHC) improved glucose metabolism in acute ischemic stroke. A total of 208 adult male Sprague Dawley rats were randomly divided into the following groups: sham, stroke, and stroke with various treatments including C + P, DHC, C + P + DHC, phloretin (glucose transporter (GLUT)-1 inhibitor), cytochalasin B (GLUT-3 inhibitor), TZD (thiazolidinedione, phosphoenolpyruvate carboxykinase (PCK) inhibitor), and apocynin (nicotinamide adenine dinucleotide phosphate oxidase (NOX) inhibitor). Stroke was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by 6 or 24 h of reperfusion. Rectal temperature was monitored before, during, and after PH. Infarct volume and neurological deficits were measured to assess the neuroprotective effects. Reactive oxygen species (ROS), NOX activity, lactate, apoptotic cell death, glucose, and ATP levels were measured. Protein expression of GLUT-1, GLUT-3, phosphofructokinase (PFK), lactate dehydrogenase (LDH), PCK1, PCK2, and NOX subunit gp91 was measured with Western blotting. PH with a combination of C + P and DHC induced faster, longer, and deeper hypothermia, as compared to each alone. PH significantly improved every measured outcome as compared to stroke and monotherapy. PH reduced brain infarction, neurological deficits, protein levels of glycolytic enzymes (GLUT-1, GLUT-3, PFK and LDH), gluconeogenic enzymes (PCK1 and PCK2), NOX activity and its subunit gp91, ROS, apoptotic cell death, glucose, and lactate, while raising ATP levels. In conclusion, stroke impaired glucose metabolism by enhancing hyperglycolysis and gluconeogenesis, which led to ischemic injury, all of which were reversed by PH induced by a combination of C + P and DHC.
Longfei Guan, Hangil Lee, Xiaokun Geng, Fengwu Li, Jiamei Shen, Yu Ji, Changya Peng, Huishan Du, Yuchuan Ding
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#35740271 2022/05/26 To Up
One Molecule for Mental Nourishment and More: Glucose Transporter Type 1-Biology and Deficiency Syndrome.Glucose transporter type 1 (Glut1) is the main transporter involved in the cellular uptake of glucose into many tissues, and is highly expressed in the brain and in erythrocytes. Glut1 deficiency syndrome is caused mainly by mutations of the gene, impairing passive glucose transport across the blood-brain barrier. All age groups, from infants to adults, may be affected, with age-specific symptoms. In its classic form, the syndrome presents as an early-onset drug-resistant metabolic epileptic encephalopathy with a complex movement disorder and developmental delay. In later-onset forms, complex motor disorder predominates, with dystonia, ataxia, chorea or spasticity, often triggered by fasting. Diagnosis is confirmed by hypoglycorrhachia (below 45 mg/dL) with normal blood glucose, 18F-fluorodeoxyglucose positron emission tomography, and genetic analysis showing pathogenic variants. There are also ongoing positive studies on erythrocytes' Glut1 surface expression using flow cytometry. The standard treatment still consists of ketogenic therapies supplying ketones as alternative brain fuel. Anaplerotic substances may provide alternative energy sources. Understanding the complex interactions of Glut1 with other tissues, its signaling function for brain angiogenesis and gliosis, and the complex regulation of glucose transportation, including compensatory mechanisms in different tissues, will hopefully advance therapy. Ongoing research for future interventions is focusing on small molecules to restore Glut1, metabolic stimulation, and transfer strategies. Newborn screening, early identification and treatment could minimize the neurodevelopmental disease consequences. Furthermore, understanding Glut1 relative deficiency or inhibition in inflammation, neurodegenerative disorders, and viral infections including COVID-19 and other settings could provide clues for future therapeutic approaches.
Romana Vulturar, Adina ChiÈ, Sebastian Pintilie, Ilinca Maria FarcaÈ, Alina Botezatu, Cristian Cezar Login, Adela-Viviana Sitar-Taut, Olga Hilda Orasan, Adina Stan, Cecilia Lazea, Camelia Al-Khzouz, Monica Mager, Mihaela Adela VinÈan, Simona Manole, Laura Damian
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#35740257 2022/05/26 To Up
IRW (Isoleucine-Arginine-Tryptophan) Improves Glucose Tolerance in High Fat Diet Fed C57BL/6 Mice via Activation of Insulin Signaling and AMPK Pathways in Skeletal Muscle.IRW (Isoleucine-Arginine-Tryptophan), has antihypertensive and anti-inflammatory properties in cells and animal models and prevents angiotensin-II- and tumor necrosis factor (TNF)-Î±-induced insulin resistance (IR) in vitro. We investigated the effects of IRW on body composition, glucose homeostasis and insulin sensitivity in a high-fat diet (HFD) induced insulin resistant (IR) model. C57BL/6 mice were fed HFD for 6 weeks, after which IRW was incorporated into the diet (45 or 15 mg/kg body weight (BW)) until week 14. IRW45 (at a dose of 45 mg/kg BW) reduced BW ( = 0.0327), fat mass gain ( = 0.0085), and preserved lean mass of HFD mice ( = 0.0065), concomitant with enhanced glucose tolerance and reduced fasting glucose ( < 0.001). In skeletal muscle, IRW45 increased insulin-stimulated protein kinase B (AKT) phosphorylation ( = 0.0132) and glucose transporter 4 (GLUT4) translocation ( < 0.001). Angiotensin 2 receptor (AT2R) ( = 0.0024), phosphorylated 5'-AMP-activated protein kinase (AMPKÎ±) ( < 0.0124) and peroxisome proliferator-activated receptor gamma (PPARÎ³) ( < 0.001) were enhanced in skeletal muscle of IRW45-treated mice, as was the expression of genes involved in myogenesis. Plasma angiotensin converting enzyme-2 (ACE2) activity was increased ( = 0.0016). Uncoupling protein-1 in white adipose tissue (WAT) was partially restored after IRW supplementation. IRW improves glucose tolerance and body composition in HFD-fed mice and promotes glucose uptake in skeletal muscle via multiple signaling pathways, independent of angiotensin converting enzyme (ACE) inhibition.
Stepheny C de Campos Zani, Myoungjin Son, Khushwant S Bhullar, Catherine B Chan, Jianping Wu
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#35739198 2022/06/23 To Up
A mathematical model of GLUT1 modulation in rods and RPE and its differential impact in cell metabolism.We present a mathematical model of key glucose metabolic pathways in two cells of the human retina: the rods and the retinal pigmented epithelium (RPE). Computational simulations of glucose transporter 1 (GLUT1) inhibition in the model accurately reproduce experimental data from conditional knockout mice and reveal that modification of GLUT1 expression levels of both cells differentially impacts their metabolism. We hypothesize that, under glucose scarcity, the RPE's energy producing pathways are altered in order to preserve its functionality, impacting the photoreceptors' outer segment renewal. On the other hand, when glucose is limited in the rods, aerobic glycolysis is preserved, which maintains the lactate contribution to the RPE.
Andrea Aparicio, Erika T Camacho, Nancy J Philp, Stephen A Wirkus
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